Data_Sheet_1_Association of soluble transferrin receptor/log ferritin index with all-cause and cause-specific mortality: National Health and Nutrition Examination Survey.docx

BackgroundSoluble transferrin receptor (sTfR)/log ferritin index (sTfR Index) can be used to assess the entire spectrum of iron status, and is valuable in evaluating iron status in population studies. There is still a lack of evidence on the association between sTfR index and all-cause mortality.ObjectTo explore the association between sTfR index and all-cause mortality, as well as mortality due to cardiovascular disease (CVD) and cancer.MethodData were from the National Health and Nutrition Examination Survey (NHANES) between 2003 to 2020. Participants aged 16 years and older who had complete data of serum ferritin and sTfR were included. Pregnant individuals or those with ineligible data on death or follow-up were excluded from the analysis. Baseline sTfR index was calculated by baseline sTfR/log (ferritin) and classified as three tertile. We performed the Cox proportional hazard regression to assess the association of sTfR index (both continuous and categorical scale) with all-cause and cause-specific mortality and further assess the non-linear relationship between sTfR index and the outcomes with restricted cubic spline.ResultIn this study, 11,525 participants, a total of 231 (2.0%) all-cause deaths occurred during a median follow-up of 51 months. The risk of all-cause mortality, CVD-related mortality, and cancer-related mortality was higher in participants with highest tertile of sTfR index. After confounding factors adjustment, participants with highest tertile of sTfR index were associated with an increased risk of all-cause mortality (HR: 1.71, 95% CI: 1.14–2.57) as compared with lowest tertile. Additionally, sTfR index per SD increment was associated with a 25% increasing risk of all-cause mortality (HR: 1.25, 95% CI: 1.08–1.45, p = 0.003) and a 38% cancer-related mortality (HR: 1.38, 95% CI: 1.07–1.77, p = 0.018). These associations remained robust after adjusting for the serum ferritin as well as in various subgroups stratified by age, sex, smoking statue, hypertension, diabetes, and CVD. Spline analysis showed that there is approximately linear relationship between sTfR index with all-cause mortality (p for non-linear = 0.481). Moreover, ferritin was not a predictor of all-cause death after adjustment for confounding factors.SignificanceThis cohort study demonstrated a significant association between sTfR index increment and an increased risk of all-cause and cancer-related mortality, independent of ferritin levels.</p

CMAP examinations 12 weeks after surgery.

<p>Representative data were recorded on the operated side of animals with plain SF/collagen scaffolds (A), TENCs (B), and autografts (C), and on the contralateral non-operated side (D). Histograms show the CMAP amplitude (E) and the motor nerve conduction velocity (F). Data are expressed as the mean ± SD. #p < 0.05 compared with the Scaffold group, and *p < 0.05 compared with the normal side.</p

Morphology of the regenerated myelinated nerve fibers.

<p>Transmission electron micrographs of the regenerated sciatic nerve (A: a1, a2). Micrographs of toluidine blue staining for the regenerated sciatic nerve under a phase contrast microscope (A: a3). The Scaffold group shows small and poorly developed regenerating clusters composed of thin, dispersed myelinated nerve fibers or non-myelinated nerve fibers. For the TENC group, the regenerated myelinated fibers dispersed densely in clusters and were surrounded by a clear, electron-dense myelin sheath and perfect basal membrane of Schwann cells. Scale bar, 2 (a1), 0.5 (a2), and 20 μm (a3). Histograms showing the number of myelin sheath layers (B) and the thickness of the myelin sheaths (C). Data are expressed as the mean ± SD. *p < 0.05 compared with the Scaffold group.</p

The gross view of sciatic nerve regeneration with different nerve grafts.

<p>The change in sciatic nerve regeneration over time (A). The normal sciatic nerve was explored, a 1-cm gap was removed, and the nerve was bridged with different nerve grafts. Examples of regenerated sciatic nerves from plain SF/collagen scaffold, TENC, autograft and control rats (B).</p

Morphology and flow cytometric analysis of ADSCs.

<p>Morphology of ADSCs under phase contrast microscopy (A). Scale bar, 100 μm (A). Flow cytometric analysis of ADSCs (B).</p

Quantitative 3D Temperature Rendering of Deep Tumors by a NIR-II Reversibly Responsive W‑VO₂@PEG Photoacoustic Nanothermometer to Promote Precise Cancer Photothermal Therapy

Accurately monitoring the three-dimensional (3D) temperature distribution of the tumor area in situ is a critical task that remains challenging in precision cancer photothermal (PT) therapy. Here, by ingeniously constructing a polyethylene glycol-coated tungsten-doped vanadium dioxide (W-VO2@PEG) photoacoustic (PA) nanothermometer (NThem) that linearly and reversibly responds to the thermal field near the human-body-temperature range, the authors propose a method to realize quantitative 3D temperature rendering of deep tumors to promote precise cancer PT therapy. The prepared NThems exhibit a mild phase transition from the monoclinic phase to the rutile phase when their temperature grows from 35 to 45 °C, with the optical absorption sharply increased ∼2-fold at 1064 nm in an approximately linear manner in the near-infrared-II (NIR-II) region, enabling W-VO2@PEG to be used as NThems for quantitative temperature monitoring of deep tumors with basepoint calibration, as well as diagnostic agents for PT therapy. Experimental results showed that the temperature measurement accuracy of the proposed method can reach 0.3 °C, with imaging depths up to 2 and 0.65 cm in tissue-mimicking phantoms and mouse tumor tissue, respectively. In addition, it was verified through PT therapy experiments in mice that the proposed method can achieve extremely high PT therapy efficiency by monitoring the temperature of the target area during PT therapy. This work provides a potential demonstration promoting precise cancer PT therapy through quantitative 3D temperature rendering of deep tumors by PA NThems with higher security and higher efficacy

Additional file 7: of miR-10a rejuvenates aged human mesenchymal stem cells and improves heart function after myocardial infarction through KLF4

Figure S6. Downregulation of miR-10a or overexpression of KLF4 in old hBM-MSCs increased apoptotic gene expression. Quantification of mRNA expression of BAX and PUMA (pr-apoptotic), BCL2 and MCL1 (antiapoptotic) in O, O-anti10a and O-KLF4 hBM-MSCs after culture for 72 h under hypoxia conditions. n = 6/group. Mean ± SD. *P < 0.05 (PDF 38 kb

Additional file 3: of miR-10a rejuvenates aged human mesenchymal stem cells and improves heart function after myocardial infarction through KLF4

Figure S2. Expression of miR-10a and KLF4 in old hBM-MSCs regulated by lentiviral vector. Lentiviral vector carrying miR-10a sequence used to transduce old hBM-MSCs (O-10a) and control vector-transduced old hBM-MSCs (O-c) served as control. miR-10a expression was significantly higher in O-10a than in control vector-transduced (O) hBM-MSCs (A). Lentiviral vector carrying KLF4 siRNA sequence used to transduce old hBM-MSCs (O-anti-KLF4). KLF4 expression was significantly lower in O-antiKLF4 than in control vector-transduced O hBM-MSCs (B). Lentiviral vector carrying anti-miR-10a sequence used to transduce old hBM-MSCs (O-anti10a). miR-10a expression was significantly lower in O-anti10a than in control vector-transduced O hBM-MSCs (C). Lentiviral vector carrying KLF4 sequence used to transduce old hBM-MSCs (O-KLF4). KLF4 expression was significantly higher in O-KLF4 than in control vector-transduced O hBM-MSCs (D). Lentivirus which carries KLF4 vector used to infect miR-10a-upregulated old hBM-MSCs (O-10a) to restore KLF4 expression (O-10a-KLF4). miR-10a-upregulated old hBM-MSCs (O-10a) also infected by the control lentivirus (O-10a-c). KLF4 expression restored in O-10a-KLF4 compared to O-10a-c hBM-MSCs (E). n = 5/group. Mean ± SD. *P < 0.05 O-c vs O-10a, O-anti-KLF4, O-anti-10a, and O-KLF4; #P < 0.05 O-10a-KLF4 vs O-10a-c and O-10a (PDF 41 kb

Additional file 1: of miR-10a rejuvenates aged human mesenchymal stem cells and improves heart function after myocardial infarction through KLF4

Table S1. qRT-PCR primer and miRNA RT primer sequences (DOCX 19 kb

Additional file 5: of miR-10a rejuvenates aged human mesenchymal stem cells and improves heart function after myocardial infarction through KLF4

Figure S4. Overexpression of miR-10a in both young and old hBM-MSCs decreased hypoxia-induced apoptosis and increased cell survival. miR-10a transduced into young (Y-10a) and old (O-10a) hBM-MSCs by lentiviral vector. Control vector-transduced young hBM-MSCs (Y-c) and old hBM-MSCs (O-c) served as controls. Cells cultured for 72 h under hypoxia conditions. (A) Cell apoptosis assayed by TUNEL staining. Percentage of apoptotic cells (TUNEL+) quantified in Y-c, Y-10a, O-c, and O-10ahBM-MSCs. (B) Cell survival evaluated in Y-c, Y-10a, O-c, and O-10a hBM-MSCs. n = 6/group. Mean ± SD. *P < 0.05, Y-c vs Y-10a; #P < 0.05, O-c vs O-10a (PDF 94 kb